Until recently, β–oxidation was believed to be exclusively located in the peroxisomes of all higher plants. Whilst this is true for germinating oilseeds undergoing gluconeogenesis, evidence demonstrating mitochondrial β–oxidation in other plant systems has refuted this central dogma of plant lipid metabolism. This report describes a comparative study of the dual mitochondrial and peroxisomal β–oxidation capacities of plant organs. Oxidation of [1–14C] palmitate was measured in the cotyledons, plumules and radicles of Pisum sativum L., which is a starchy seed, over a 14 day period from the commencement of imbibition. Respiratory chain inhibitors were used for differentiating between mitochondrial and peroxisomal β–oxidation. Peroxisomal β–oxidation gave a steady, baseline rate and, in the early stages of seedling development, accounted for 70–100% of the β–oxidation observed. Mitochondrial β–oxidation gave peaks of activity at days 7 and 10–11, accounting for up to 82% of the total β–oxidation activity at these times. These peaks coincide with key stages of seedling development and were not observed when normal development was disrupted by growth in the dark. Peroxisomal β–oxidation was unaffected by etiolation. Since mitochondrial β–oxidation was overt only during times of intense biosynthetic activity it might be switched on or off during seedling development. In contrast, peroxisomes maintained a continuous, low β-oxidation activity that could be essential in removing harmful free fatty acids, e.g. those produced by protein and lipid turnover.